Fig. 1

Autophagy is an evolutionarily conserved stress response that is upregulated by a range of cellular stressors, including fasting as well as various pro-inflammatory signals. In turn, this catabolic process may be dynamically repurposed to resolve a range of cellular stresses that may emerge during sepsis. This includes the removal of large protein structures as well as remodelling of the proteome to better accommodate emerging stressors faced during sepsis. ER-phagy as well as aggrephagy plays a role in preventing the accumulation of toxic protein aggregates, whereas xenophagy represents an indispensable mechanism in cell-autonomous defence against intercellular pathogens. Autophagy is also involved in the processing and presentation of both endogenous and exogenously derived epitopes, thereby playing a potential role in regulating the immunogenicity of infected cells. Autophagy also has a well-established role in reshaping the proteome. As an example, recent findings in cancer cells revealed an exquisite selectivity in the pool of proteins targeted for degradation and that such remodelling of the proteome may promote cell survival by attenuating inflammatory processes